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A 60 yo with 2 previous inferior (RCA) STEMIs, stented, called 911 for one hour of chest pain. Here is his most recent previous ECG: This was recorded after intervention for inferior STEMI (with massive ST Elevation, see below), and shows inferior Q-waves with T-wave inversion typical of completed inferior OMI. ng/mL (quite large).
Despite anticipation by many that the initial post-resuscitation ECG will show an obvious acute infarction — this expected "STEMI picture" is often not seen. Meyers and Smith in the October 15, 2022 post of Dr. Smith's ECG Blog ). 15, 2022 post). Indeed, careful attention to detail is needed to appreciate the important findings.
So while there’s no diagnostic STEMI criteria, there are multiple ischemic abnormalities in 11/12 leads involving QRS, ST and T waves, which are diagnostic of a proximal LAD occlusion. First trop was 7,000ng/L (normal 25% of ‘Non-STEMI’ patients with delayed angiography have the exact same pathology of acute coronary occlusion.
Cath lab declined as it is not a STEMI." And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mindset. Do NOT give it unless you are committed to the cath lab!! Cath attending is aware. Abstract 556.
However, whether immediate blood glucose and FIB levels affect coronary blood flow during primary percutaneous coronary intervention (PCI) remains unclear.ObjectiveTo explore the correlation between admission blood glucose (ABG), fibrinogen (FIB) and slow blood flow during primary PCI for acute ST segment elevation myocardial infarction (STEMI).MethodsA
The ECG did not meet STEMI criteria, and the final cardiology interpretation was “ST and T wave abnormality, consider anterior ischemia”. There’s only minimal ST elevation in III, which does not meet STEMI criteria of 1mm in two contiguous leads. But STEMI criteria is only 43% sensitive for OMI.[1]
Cardiogenic shock (CS)is the most feared event following STEMI. We tend to perceive CS as an exclusive complication of STEMI. The incidence is half of that of STEMI, i.e., 2.5-5%. might show little elevation with considerable overlap of left main STEMI vs NSTEMI ) 2.Onset 2022 Jun 20;11(12):3558. Reference 1.Martínez
I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion. Non-STEMI guidelines call for “urgent/immediate invasive strategy is indicated in patients with NSTE-ACS who have refractory angina or hemodynamic or electrical instability,” regardless of ECG findings.[1]
The interventional cardiologist then canceled the activation and returned the patient to the ED without doing an angiogram ("Not a STEMI"). I advised that perhaps posterior leads would help to persuade the interventionalist, since the 2022 ACC recommendations include posterior STEMI as a formal STEMI equivalent, but only officially by 0.5
I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict: You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form Then I learned that a Code STEMI was activated for concern of anterior "STEMI" in V1-V2. High sensitivity troponin I was 23 ng/L.
Take home messages: 1- In STEMI/NSTEMI paradigm you search for STE on ECG. If this patient was managed according to the STEMI/NSTEMI paradigm (although he would be a candidate for early invasive treatment), he would probably be taken to the cath lab hours later. Here is the post-intervention angiogram and post-PCI ECG. 2021.21026.
If we took this as the gold standard, we would conclude that the computer interpretation was safe and accurate at least accurate enough to not miss STEMI, and that physicians should not be interrupted to interpret it, because there would be no change in patient management. What is the gold standard for ECG interpretation: patient outcome!!!
4,5] We have now formally studied this question: Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review.[6] have published a number of warnings about the previous reassuring studies.[4,5]
Its hard to measure the STE in I exactly with the moving baseline, but there is almost certainly not enough STE to meet STEMI criteria. The ACC recognizes these findings as formal STEMI equivalents (though they do not define how to find them). They are symmetric, fat, convex on both sides, etc.
Notice on the right side of the image how the algorithm correctly measures STE sufficient in V1 and V2 to meet STEMI criteria in a man older than age 40. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Thus, this is obvious STEMI(+) OMI until proven otherwise.
Despite the absence of significant coronary stenosis on her post-arrest cath — the ECG in Figure-1 is clearly diagnostic of an extensive anterolateral STEMI ( presumably from acute LAD [ L eft A nterior D escending ] coronary artery occlusion). The rhythm in ECG #1 is regular and supraventricular at a rate of ~75/minute.
This is diagnostic of infero-posterior OMI, but it is falsely negative by STEMI criteria and with falsely negative posterior leads (though they do show mild ST elevation in V4R). They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS. Figure-1: The initial ECG in today’s case.
Unknown algorithm The Queen gets it right Case 4 How unreliable are computer algorithms in the Diagnosis of STEMI? The patient's prehospital ECG showed that there was massive STEMI and these are hyperacute T-waves "on the way down" as they normalize. Pain was resolving. Diagnosed as Normal by the computer. Troponin negative.
Background Despite the crucial role of Chest pain centers (CPCs) in acute myocardial infarction (AMI) management, China's mortality rate for ST-segment elevation myocardial infarction (STEMI) has remained stagnant. Conclusion CPC quality control metrics affect STEMI mortality based on Killip class.
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later? This caused a type 2 anterior STEMI. The April 8, 2022 post by Drs.
This was a machine read STEMI positive OMI. The meaning of this quote is that at times, something as obvious as the dramatic anterior lead ST elevation that we see in today's tracing is not the result of an acute LAD STEMI. His ECG is shown below. Pretty obvious anterior current of injury. What would you guess is the culprit artery?
Subtle as a STEMI." (i.e., Here is the bottom line of the article: It is widely believed that hyperacute T-waves are a transitional state preceding ST Elevation 1–4 Thus, it is tempting to postulate that early cases of OMI will eventually evolve to STEMI; yet, our data contradicts that notion. This one is easy for the Queen.
A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. The two cases were considered: Patient 1 was recognized by the ED provider and the cardiologist as having resolved “STEMI”. He wrote most of it and I (Smith) edited.
Patient still not having chest pain however this is more concerning for OMI/STEMI. Wellens' syndrome is a syndrome of Transient OMI (old terminology would be transient STEMI). As far as I can tell, there is only one randomized trial of immediate vs. delayed intervention for transient STEMI. Labs ordered but not yet drawn.
The Minneapolis Heart Institute Foundation (MHIF) is presenting leading research focused on trends in ST-elevation myocardial infarction (STEMI), the most severe form of a heart attack, at the American College of Cardiology’s Annual Scientific Session (ACC.24), 24), being held April 6-8 in Atltanta, GA.
Methods Clinical data from patients admitted to the cardiology division between 2018 and 2022, who were diagnosed with AMI and underwent an IPF testing. Results Among the 277 patients diagnosed with AMI who underwent IPF testing, 113 had (STEMI) and 164 had (NSTEMI). Notably, among STEMI patients, those with IPF ≥ 4.2%
Here they are: Patient 1, ECG1: Zoll computer algorithm stated: " STEMI , Anterior Infarct" Patient 2, ECG1: Zoll computer algorithm stated: "ST elevation, probably benign early repolarization." He diagnosed anterior "STEMI" and activated the cath lab. 25 minutes later, EMS called back with this new ECG: Super obvious STEMI(+) OMI.
The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
P utting I t A ll T ogether : After correcting for LA-LL lead reversal — ECG # 1a shows sinus rhythm — LVH — and an acute infero-postero STEMI with acute RV involvement. PEARL # 3: In the absence of an anterior STEMI — acute inferior MI is the result of either acute RCA or LCx ( L eft C ircumfle x ) coronary occlusion.
In the available view of the sinus rhythm, we see normal variant STE which probably meets STEMI criteria in V4 and V5. In other words, the inferior "ST elevation" is due to the abnormal rhythm, and does not signify OMI or STEMI in any way. This situation has been named "Emery phenomenon." YOU TOO CAN HAVE THE PM Cardio AI BOT!!
STEMI MINOCA versus NSTEMI MINOCA STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at al. Circulation. 2017;135(16):1490–3.
Recall from this post referencing this study that "reciprocal STD in aVL is highly sensitive for inferior OMI (far better than STEMI criteria) and excludes pericarditis, but is not specific for OMI." Immediate versus delayed invasive intervention for non-stemi patients. Is there anything else on the tracing to corroborate inferior OMI?
This is documented as a STEMI in the clinical notes and in the cath report, but certainly does not meet STEMI criteria and is therefore an NSTEMI by definition. For national registry purposes, this will be incorrectly classified as a STEMI.) Most STEMI have peak cTnI greater than 10.0. Large STEMI are approximately 30-80.
There is an obvious inferior posterior STEMI(+) OMI. Methods Retrospective study of consecutive inferior STEMI , comparing ECGs of patients with, to those without, RVMI, as determined by angiographic coronary occlusion proximal to the RV marginal branch. The April 17, 2022 post ( Leads V1,V2 misplacement ). How would one tell?
In the October 15, 2022 post of Dr. Smith's ECG Blog — Drs. Smith and Meyers in their October 15, 2022 post on Precordial Swirl. Figure-3: Selected sets of V1,V2 leads from the examples of Precordial Swirl provided in the October 15, 2022 post in Dr. Smith's ECG Blog. What is P recordial S wirl ?
This is guideline approved by both ACC/AHA and by European guidelines. == Comment by K EN G RAUER, MD ( 6/1/2022 ): == I found serial evaluation of sequential tracings in today's case to be subtle — yet highly insightful. A patient with active chest pain and an otherwise unexplained elevated troponin should go to the cath lab.
It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. A mong patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common.
It may look identical t o the ST-T wave appearance seen after a STEMI with marked troponin elevation, that has now reperfused ( be this reperfusion spontaneous — or by treatment with PCI or thrombolytics ). A DDENDUM ( 10/26/2024 ) : I excerpted what follows below from My Comment in the August 12, 2022 post in Dr. Smith's ECG Blog ). =
The conventional machine algorithm interpreted this ECG as STEMI. See this post of RV MI with both McConnell sign and "D" sign: Inferior and Posterior STEMI. She was out walking her dog when she developed sudden dizziness and light-headedness. When EMS found her, she was dyspneic and diaphoretic.
Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1] But it is still STEMI negative. A 15 lead ECG was done (below). In a study last year, 14.4%
Will evolve into STEMI by prothrombotic trigger of lytic agent ECG will get normalised with clinical stability in some Nothing happens. Majority of Wellens end up as NSTEMI, statistics tells us about 20% of them can be STEMI in incognito mode demanding lysis or emergency PCI. BMC Cardiovasc Disord 22 , 176 (2022). Reference 1.
But because there was no new ST elevation, the ECG was signed off as “STEMI negative” and the patient waited to be seen. But the ECG still doesn’t meet STEMI criteria. It was therefore interpreted as “no STEMI” and the patient was treated with dual anti-platelets and referred to cardiology as “NSTEMI.” the cardiologist 5.
Here, I do not see OMI (although the ECG is falsely STEMI positive with just over 1 mm STE in V1 and about 2.5 The April 17, 2022 post ( Leads V1,V2 misplacement ). The May 5, 2022 post ( LA-RA reversal ). The May 24, 2022 post ( LA-LL reversal ). The May 26, 2022 post ( LA-LL reversal ). What do you think?
His EKG with worse pain now shows enough ST elevation to meet STEMI criteria. The EKG was read by the conventional computer algorithm as diagnostic of “ACUTE MI/STEMI”. The patient started receiving medications for “STEMI” (including heparin!!!) The patient started receiving medications for “STEMI” (including heparin!!!)
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